Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells

Mark Kaplan, Ulrike Schindler, Stephen T. Smiley, Michael J. Grusby

Research output: Contribution to journalArticle

1236 Citations (Scopus)

Abstract

Interleukin-4 (IL-4) stimulation of cells leads to the activation of multiple signaling pathways, one of which involves Stat6. We have generated Stat6-deficient mice by gene targeting in embryonic stem cells to determine the role of this transcription factor in mediating the biologic functions of IL-4. IL-4-induced increases in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrogated, and lymphocytes from Stat6-deficient animals fail to proliferate in response to IL-4. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. In addition, Stat6-deficient T lymphocytes fail to differentiate into Th2 cells in response to either IL-4 or IL-13. These results demonstrate that, despite the existence of multiple signaling pathways activated by IL-4, Stat6 is essential for mediating responses to IL-4 in lymphocytes.

Original languageEnglish (US)
Pages (from-to)313-319
Number of pages7
JournalImmunity
Volume4
Issue number3
DOIs
StatePublished - Mar 1996
Externally publishedYes

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Th2 Cells
Interleukin-4
Interleukin-4 Receptors
Lymphocytes
Interleukin-13
Gene Targeting
Histocompatibility Antigens Class II
Embryonic Stem Cells
Immunoglobulin E
Immunization
B-Lymphocytes
Transcription Factors
T-Lymphocytes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

Cite this

Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells. / Kaplan, Mark; Schindler, Ulrike; Smiley, Stephen T.; Grusby, Michael J.

In: Immunity, Vol. 4, No. 3, 03.1996, p. 313-319.

Research output: Contribution to journalArticle

Kaplan, Mark ; Schindler, Ulrike ; Smiley, Stephen T. ; Grusby, Michael J. / Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells. In: Immunity. 1996 ; Vol. 4, No. 3. pp. 313-319.
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